David A. Brenner
University of California, San Diego
Internal medicineEndocrinologyPathologyMolecular biologyHepatic stellate cellTumor necrosis factor alphaChemistryApoptosisImmunologyLiver injuryCirrhosisFatty liverFibrosisHepatic fibrosisCancer researchBiochemistryMedicineBiologyGastroenterologyCell biology
610Publications
149H-index
47.3kCitations
Publications 606
Newest
#1David A. Brenner (Heidelberg University)H-Index: 149
#2Kathrin Muller (University of Ulm)H-Index: 19
Last. Jochen H. Weishaupt (Heidelberg University)H-Index: 29
view all 9 authors...
Mutations in FUS and TBK1 often cause aggressive early-onset amyotrophic lateral sclerosis (ALS) or a late-onset ALS and/or frontotemporal dementia (FTD) phenotype, respectively. Co-occurrence of mutations in two or more Mendelian ALS/FTD genes has been repeatedly reported. However, little is known how two pathogenic ALS/FTD mutations in the same patient interact to shape the final phenotype. We screened 28 ALS patients with a known FUS mutation by whole-exome sequencing and targeted evaluation ...
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#1Takahiro Nishio (UCSD: University of California, San Diego)H-Index: 15
#2Yukinori Koyama (Kyoto University)H-Index: 35
Last. Keiko Iwaisako (Dodai: Doshisha University)H-Index: 25
view all 17 authors...
We investigated the role of mesothelin (Msln) and thymocyte differentiation antigen 1 (Thy1) in the activation of fibroblasts across multiple organs and demonstrated that Msln-/- mice are protected from cholestatic fibrosis caused by Mdr2 (multidrug resistance gene 2) deficiency, bleomycin-induced lung fibrosis, and UUO (unilateral urinary obstruction)-induced kidney fibrosis. On the contrary, Thy1-/- mice are more susceptible to fibrosis, suggesting that a Msln-Thy1 signaling complex is critica...
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#1Francisco I. Ramirez-Perez (MU: University of Missouri)H-Index: 13
#2Makenzie L. Woodford (MU: University of Missouri)H-Index: 7
Last. Bysani ChandrasekarH-Index: 58
view all 11 authors...
Arterial stiffening, a characteristic feature of obesity and type 2 diabetes, contributes to the development and progression of cardiovascular diseases (CVD). Currently, no effective prophylaxis or therapeutics is available to prevent or treat arterial stiffening. A better understanding of the molecular mechanisms underlying arterial stiffening is vital to identify newer targets and strategies to reduce CVD burden. A major contributor to arterial stiffening is increased collagen deposition. In t...
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#1Gavin E. Arteel (University of Pittsburgh)H-Index: 57
#2Tatiana Kisseleva (UCSD: University of California, San Diego)H-Index: 45
Last. David A. Brenner (UCSD: University of California, San Diego)H-Index: 149
view all 12 authors...
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#1Jacopo Baglieri (UCSD: University of California, San Diego)H-Index: 8
#2Cuili Zhang (UCSD: University of California, San Diego)H-Index: 1
Last. Jidong Jia (Capital Medical University)H-Index: 38
view all 14 authors...
Although hepatocellular cancer (HCC) usually occurs in the setting of liver fibrosis, the causal relationship between liver fibrosis and HCC is unclear. By studying in vivo and in vitro models of HCC using Colr/r mice (that produce a collagenase resistant Type I collagen) or WT mice, we aim to assess the relationship between Type I collagen, liver fibrosis, and experimental HCC. HCC was either chemically induced in WT and Colr/r mice or Hepa 1-6 cells were engrafted into WT and Colr/r livers. Th...
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#1Souradipta Ganguly (UCSD: University of California, San Diego)H-Index: 2
#2German R. Aleman Muench (Janssen Pharmaceutica)H-Index: 4
Last. Debanjan Dhar (UCSD: University of California, San Diego)H-Index: 20
view all 16 authors...
BACKGROUND & AIMS How benign liver steatosis progresses to non-alcoholic steatohepatitis (NASH), fibrosis and hepatocellular carcinoma (HCC) remains elusive. NASH progression entails diverse pathogenic mechanisms and relies on complex cross-talk between multiple tissues such as the gut, adipose tissues, liver and the brain. Using a hyperphagic mouse fed with Western diet (WD), we aimed to elucidate the cross-talk and kinetics of hepatic and extra-hepatic alterations during NASH-HCC progression a...
1 CitationsSource
#1Michael KarinH-Index: 257
#2Cristina LlorenteH-Index: 13
Last. Bernd SchnablH-Index: 65
view all 18 authors...
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#1Wouter van Rheenen (UU: Utrecht University)
Last. Nayana GaurH-Index: 5
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a life-time risk of 1 in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry GWAS in ALS including 29,612 ALS patients and 122,656 controls which identified 15 risk loci in ALS. When combined with 8,953 whole-genome sequenced individuals (6,538 ALS patients, 2,415 controls) and the largest cortex-derived eQTL dataset (MetaBrain), analyses revealed locus-specific genetic architect...
5 CitationsSource
#1Tatiana Kisseleva (UCSD: University of California, San Diego)H-Index: 45
#2David A. Brenner (UCSD: University of California, San Diego)H-Index: 149
Chronic liver injury leads to liver inflammation and fibrosis, through which activated myofibroblasts in the liver secrete extracellular matrix proteins that generate the fibrous scar. The primary source of these myofibroblasts are the resident hepatic stellate cells. Clinical and experimental liver fibrosis regresses when the causative agent is removed, which is associated with the elimination of these activated myofibroblasts and resorption of the fibrous scar. Understanding the mechanisms of ...
48 CitationsSource
#1Sara Brin Rosenthal (UCSD: University of California, San Diego)H-Index: 15
#2Xiao Liu (UCSD: University of California, San Diego)H-Index: 19
Last. David A. Brenner (UCSD: University of California, San Diego)H-Index: 149
view all 11 authors...
In clinical and experimental non-alcoholic steatohepatitis (NASH), the origin of the scar-forming myofibroblast is the hepatic stellate cell (HSC). We used foz/foz mice on a Western diet to characterize in detail the phenotypic changes of HSCs in a NASH model. We examined the single cell expression profiles (scRNA-Seq) of HSCs purified from the normal livers of foz/foz mice on a chow diet, in NASH with fibrosis of foz/foz mice on a Western diet, and in livers during regression of NASH after swit...
6 CitationsSource